Using a tiny flatworm best known for its extraordinary ability to regenerate lost tissue, researchers have identified a gene that controls the ability of stem cells to differentiate into specialized cells. The gene encodes a protein that is most similar to the protein PIWI, an important regulator of stem cells in organisms ranging from plants to humans.
The replacement of tissue lost to injury or shed during the bodys normal activities is essential for the survival of most organisms. The new study, published in the November 25, 2005, issue of the journal Science, helps scientists understand how stem cells make this process possible. The research, performed at the University of Utah School of Medicine, was carried out by Helen Hay Whitney postdoctoral fellow Peter W. Reddien (now an Associate Member at the Whitehead Institute for Biomedical Research), and led by Howard Hughes Medical Institute investigator Alejandro Sánchez Alvarado.
Salamanders, zebrafish, and other organisms are capable of regenerating entirely new body parts. Although the human body does not face such demands, it is constantly replacing lost cells. For example, blood replenishes itself, wounds heal, and the lining of the gut sloughs off and is restored. Nowhere, however, is the process of regeneration more dramatic than in the freshwater flatworm planaria. Cut one of these animals in half, and a week later, two fully functional worms will have developed from the pieces. Cut a piece that is 1/279th the size of the animal, and it too will regrow into a complete worm.
Jennifer Michalowski | EurekAlert!
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Many pathogens use certain sugar compounds from their host to help conceal themselves against the immune system. Scientists at the University of Bonn have now, in cooperation with researchers at the University of York in the United Kingdom, analyzed the dynamics of a bacterial molecule that is involved in this process. They demonstrate that the protein grabs onto the sugar molecule with a Pac Man-like chewing motion and holds it until it can be used. Their results could help design therapeutics that could make the protein poorer at grabbing and holding and hence compromise the pathogen in the host. The study has now been published in “Biophysical Journal”.
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